status of the efflux theory

[Guest guest]

OK, so its not really a theory, more of a logical possiblity.

The persistent Chlamydiae trachomatis found in chlamydial ReA were

shown by Nanagara to have little LPS, in vivo. The same is true, in

glass, of L-forms of several bacterial species. LPS is lipophobic and

protects the cell from lipophilic molecules. Therefore, these LPS-

deficient cells are rather naked (unless they have replaced LPS with

some other lipophobe).

There are probably a whole lot of hostile lipophilic molecules in the

leucocyte plasm where the Wirostko uveitis L-forms are. Perhaps there

are also alot where the ReA chlamydiae are. Therefore, whatever

motivates the bugs to " go naked " (possibly immunoevasion), they may

have a real problem getting barraged with lipophilic toxins. This

could motivate sizable up-regulation of nonspecific efflux pumps

which would also dump our beloved antimicrobials, preventing them

from kicking ass.

It seems most bacteria have such pumps, and Mtb and P. aeruginosa, at

least, have the capacity to upregulate them at least 10x during toxic

attack - this without undergoing any mutations, but in accordance

with design.

There is still nothing to directly indicate that this is whats

happening, and this still begs alot of glaring questions. Ive only

gone into the parts that fit together well; other parts dont, but at

this point I still think its possible they could be crammed together,

um, I mean discovered to fit together.

For one thing, spirochaetales like Tp and Bb dont have LPS at all,

not in any morphologic variant.